Training at altitude is a method widely used by athletes to enhance their endurance and performance at sea level (1). Studies in the athletic literature suggest that simulated altitude exposure, utilizing hypoxic devices, may have a similar benefit (2, 3). The improved performance achieved by altitude exposure is thought to be due to the physiological changes that occur during acclimatization (1).
Several physiological changes occur during ascent to altitude from sea level. These changes are primarily due to the reduced partial pressure of inspired oxygen secondary to changes in barometric pressure with altitude (4, 5). Physiological changes with altitude usually appear above 2300-2800 meters (6). Within minutes of ascent to an altitude, circulatory and respiratory changes occur (4). Continued stay at the higher altitude leads to acclimatization, a process of physiological adjustment leading to adaptation to the changed altitude.
Studies in athletes suggest that improved exercise capacity with altitude exposure may be due to the changes in blood volumes and oxygen handling capacity of the red blood cells. During acclimatization, there is an erythropoietin induced increase in red blood cell mass in response to hypoxia. In addition, there is a rightward shift of the oxy-hemoglobin dissociation curve with increase in 2, 3-diphospoglycerate level. Right shift of the curve leads to reduced affinity for oxygen, and hence, improved tissue oxygenation (4).
Ventilatory changes also occur in response to acclimatization. There is an increase in ventilation, mainly due to an increase in tidal volume. This hypoxic ventilatory response also improves oxygen transportation (4). Furthermore, biochemical and structural changes in skeletal muscle occur and an increase in capillary density is found after exposure to high altitude. (4).
Altitude exposure may have a favorable effect on cardiac function as well. An interesting study by Liu et al, showed improvement in left ventricular and systolic diameter and stroke volume in a group of altitude trained athletes (7). Altitude induced hypoxia may lead to cardio protective effects against ischemic and reperfusion injury (8, 9). In another study, altitude adapted chinchilla rabbits showed activation of gene signaling that lead to prevention of hypertrophy in a pressure overload model (10).
Reduced exercise capacity is a dominant finding in heart failure. Several structural and functional abnormalities have been shown in skeletal muscle in patients with end stage heart failure, which may contribute to reduced exercise capacity (11, 12, 13). Heart failure is associated with impaired oxygen delivery to the periphery, and this may further contribute to impaired exercise capacity. Furthermore, increasing hemoglobin concentration has been shown to improve exercise capacity, which is likely related to improved oxygen delivery (14, 15).
Agostoni et al studied the acute effect of simulated altitude (up to 3000 m) on exercise capacity in heart failure patients. There was a reduction in exercise capacity during exercise at altitude for both normal subjects and those with heart failure. This acute exposure to altitude during the stress test was well tolerated in patients with advanced heart failure (peak VO2<15 ml/kg/min) (16). Another study of patients with ischemic cardiomyopathy showed that acute exposure to altitude (2500 m) during exercise was well tolerated. In the prior two studies, there were no episodes of significant arrhythmia (17). Moreover, commercial airplane pressure conditions are equivalent to 2400 meters and airplane travel is considered safe for stable patients with heart failure (18, 19).